Sunday, 25 March 2018

B regulatory cells promote remyelination

First we had T regulatory cells promoting remyelination. 

In this report it is the turn of the B regulatory cells to do the same thing
Tanabe S, Yamashita T. B-1a lymphocytes promote oligodendrogenesis during brain development.Nat Neurosci. 2018 Mar 5. doi: 10.1038/s41593-018-0106-4. [Epub ahead of print]

During brain development, the immune system mediates neurogenesis, gliogenesis and synapse formation. However, it remains unclear whether peripheral lymphocytes contribute to brain development. Here we identified the subtypes of lymphocytes that are present in neonatal mouse brains and investigated their functions. We found that B-1a cells, a subtype of B cells, were abundant in the neonatal mouse brain and infiltrated into the brain in a CXCL13–CXCR5-dependent manner. B-1a cells promoted the proliferation of oligodendrocyte-precursor cells (OPCs) in vitro, and depletion of B-1a cells from developing brains resulted in a reduction of numbers of OPCs and mature oligodendrocytes. Our results demonstrate that B-1a cells infiltrate into the brain and contribute to oligodendrogenesis and myelination by promoting OPC proliferation via IgM–Fc Receptor signaling.

We have heard about regulatory T cells promoting oligodendrocyte health, in this report it says that at least in mice there are B cells that accumulate in the brain and promote oligodendrocyte development.

In this study they say that B1a, B cells are present in the brain early after birth and influence oligodendrocyte development.

B1 cells are a sub-class of B cell lymphocytes that have no memory, but otherwise, B1 cells perform many of the same roles as other B cells: making antibodies against antigens and acting as antigen presenting cells

B1 cells are first produced in the foetus and most B1 cells undergo self-renewal in the periphery, unlike conventional B cells (B2 cells) that are produced after birth and replaced in the bone marrow.

Human B1 cells were found to have marker profile of CD20+CD27+CD43+CD70- and could either be CD5+ or CD5-.
Mouse B cells are more complex than human cells, B-1 B cells, in the mouse, can be further subdivided into B-1a (CD5+) and B-1b (CD5−) subtypes but the problem is are these a mouse issue without any clear human correlate. So the question is whether the have the same functions.

In the mouse, CD5 is expressed by microglia in humans they do not.  The CD5+ B1a cells have been suggested to be B regulatory cells.

Clearly it will be a growth factor(s), but which ones?


  1. What does this mean / ramifications
    for people on Ocrelizumab?

  2. If they exist in humans then they get depleted with ocrelizumsb. There are bound to be good and bad B cells but on balance getting rid of the bad is probably what's needed

  3. "We have heard about regulatory T cells"

    You dont need them anymore :)

    "We show that the allegedly 'professional class' of immunosuppressive Tregs is not necessarily the key player in resolving inflammation in this experimental model," says von Herrath, a professor in LJI's Division of Developmental Immunology. "We now find that many cells, among them non-specific CTLs, can do that"

    That idea that Tregs are the dedicated inflammation fighters is so entrenched in the field that the group performed experiments proving that protection conferred by bystanders had nothing to do with expanding Treg populations. "Tregs do have profound anti-inflammatory effects in some disease models," says Christoffersson. "But treatments seeking to expand this cohort of cells have not proven as successful in the clinic as they have been in the lab."

    Von Herrath says his colleagues in the field must now recognize that diverse immune cell types, not just Tregs, can potentially rein in the inflammatory response in autoimmune disease. "In the end 'professional Tregs' may matter less than we thought," he says. Von Herrath also relishes how his new paper upends dogma in the field. "Right now people are talking about challenges to science," he says. "But the biggest threat to science comes when we hold onto ideas too closely. Then we might miss the obvious."

  4. What's happened to Prof G? Has he given up on the blog?


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